Author

R. Lupo

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 4

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 4 Approach:experimental assay· 4 Organism:mouse· 4 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:metabolomics· 1 Assay:proteomics· 1

Frequent Co-Authors

J. V. Alvarez· 4 shared R. Newcomb· 3 shared A. Walens· 2 shared D. B. Fox· 2 shared J. S. Damrauer· 2 shared N. W. Mabe· 2 shared A. V. DiMarco· 1 shared B. A. Vilona· 1 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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4 shared papersCancer Biology

J. V. Alvarez

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Author profile →

4 papers

Recent·Most cited

Adaptation and Selection Shape Clonal Evolution During Residual Disease and Recurrence

A. Walens, J. Lin, J. S. Damrauer, R. Lupo, R. Newcomb, D. B. Fox, N. W. Mabe, J. Gresham, T. De Buysscher, H. Kelkar, P. Mieczkowski, K. Owzar, J. V. Alvarez

This study tracks clonal evolution in residual breast cancer tumors and finds that recurrence can arise through distinct evolutionary paths with different clonal compositions and drug sensitivities.

bioRxiv · Apr 22, 2020Cancer Biology

G9a Promotes Breast Cancer Recurrence Through Repression of a Pro-inflammatory Program

N. W. Mabe, S. E. Wolery, R. Newcomb, R. C. Meingasner, B. A. Vilona, C.-C. LIN, R. Lupo, J.-T. A. Chi, J. V. Alvarez

This study shows that G9a promotes breast cancer recurrence by repressing pro-inflammatory genes, leading to necroptosis when inhibited.

bioRxiv · Jan 9, 2020Cancer Biology

CCL5 promotes breast cancer recurrence through macrophage recruitment in residual tumors

A. Walens, A. V. DiMarco, R. Lupo, B. R. Kroger, J. S. Damrauer, J. V. Alvarez

This study identifies CCL5 as a factor promoting breast cancer recurrence by recruiting macrophages in residual tumors following Her2 downregulation.

bioRxiv · Apr 11, 2019Cancer Biology

NRF2-dependent metabolic reprogramming is required for tumor recurrence following oncogene inhibition

D. B. Fox, R. Lupo, L. C. Noteware, R. Newcomb, J. Liu, J. W. Locasale, M. D. Hirschey, J. V. Alvarez

This study identifies NRF2-driven metabolic reprogramming as essential for breast cancer recurrence after oncogene inhibition and shows it can be targeted with glutaminase inhibitors.

bioRxiv · Jan 8, 2019 · PreprintCancer Biology